Introduction: Hashimoto's disease is a chronic, autoimmune disease characterized by the appearance of autoreactive lymphocytes and anti-thyroid antibodies, which mediate progressive thyroid destruction. A significant proportion of the lymphocytic thyroid infiltrate consists of CD4+ and CD8+ T lymphocytes, whose development, differentiation and function are controlled by small non-coding microRNA molecules, hsa-let7a, hsa-miR-20a, hsa-miR-106a and hsa-miR-301a. Study aim: To examine transcriptional profiles of hsa-let7a, hsa-miR-20a, hsa-miR-106a and hsa-miR-301a in peripheral blood T lymphocytes of HT patients and to determine their association with age, thyroid volume, levels of TSH, FT3, FT4 and anti-TPO in serum samples and replacement L-T4 therapy. Material and methods: The study included a collection of archive RNA samples isolated from peripheral blood T lymphocytes of 13 healthy controls and 33 HT patients. The cDNA synthesis was performed with use of TaqMan Advanced microRNA cDNA Synthesis Kit, whereas miRNA expression levels were assessed by quantitative real-time PCR reaction (qRT-PCR) in a Quant Studio 5 instrument usin TaqMan Advanced miRNA expression assays. Results: Compared to euthyroid patients and healthy controls, peripheral blood T lymphocytes of hypothyroid subjects exhibit a significantly lower hsa-miR-106a-5p expression. Moreover, decreased has-miR-106a-5p expression correlates with the increased RORC gene expression in treated and untreated hypothyroid patients. Conclusion: Dysregulated hsa-miR-106a-5p/RORC circuit potentially play a role in the development of an uncontrolled type 17 immune response in Hashimoto's disease.